Cybernetic Physiology and Internal Medicine
by Alexandra Spar
Summary: A text written by Alirion (once Alirion Victrix, of Amaranth) regarding the physiology of Transformers and the intricacies of TF clinical treatment.
1. Circulovascular Systems

Disclaimer: I do not own "Transformers," nor any characters or related indicia thereof. No money is being made and no copyright infringement is intended.

This is the first chapter of a guide written by Alirion of Frey's Hope for the use of other medics in the treatment of Cybertronians and other cybernetic lifeforms. Guided toward the neophyte in cybermedicine. This will probably not interest you.

Cybernetic Physiology and Internal Medicine

1) Overview

The cybernetic races possess a distinct and individualistic physiology which both parallels and diverges from organic humanoid physiology. Analogous systems exist in the two basic models, but the importance of each system is specific to the species, rather than as a general rule of thumb. As the Cybertronian race of cybernetic lifeforms is the most commonly encountered, it is this basic model we will be using in our discussion.  
  
2.) Circulatory/Fuel Systems

2i. The Cybertronian physiology features two discrete but related circulatory systems, the fuel system and the circulating coolant system. These serve different but related purposes. The fuel system comprises the energon intake, holding and conversion tanks, and the distributary conduits that provide fuel to the body's systems. The main energy distribution pathway in the body is via wiring: fuel is consumed—either orally or intraconduitally--, converted into electrical energy, and held in central batteries which power the individual between fuel intakes. However, the various musculoskeletal systems—separated for multiple redundancy to ensure that damage to one sector of the body does not result in widespread deactivation of systems—have their own liquid fuel supply and conversion modules. This auxiliary energon supply is recirculated via a small pump located below the main energon conversion tanks. Thus, if damage or blockage to the main cable bus feeding power to a limb prevents mainline power transfer, the auxiliary energon feed systems will allow that limb to continue functioning without interruption.

Once the fuel has been processed through the conversion tanks, changing the electrical potential in the liquid energon into electrical energy, the liquid matrix remains. This liquid now passes through a filtration barrier into the circulating coolant fluid reservoir, combining with the CLA (q.v) in the coolant fluid, and is pumped out into the circulovascular cooling network.

The circulating coolant system is the most vital of the basic somatic functions of the Cybertronian physiology. While in deep interstellar space, the heat produced by normal functioning is able to disperse through the external armour plating; however, in temperature ranges above 273 degrees Kelvin/0 degrees Celsius, heat transfer is required to maintain optimal functioning efficiency. Thus, a liquid coolant network draws heat away from the circuitry and disperses it via heat-transfer modules located close to the external surface. The coolant fluid itself is contained within a vascular network of conduits which are capable of expanding and contracting to adjust flow and pressure within the system. This vascular tension is autonomically controlled, and the stimuli which cause these autonomic corrections can be artificially induced to produce particular effects.

The conversion process which transforms the energy matrix present in energon into usable electrical power produces a great deal of heat as a byproduct; therefore the vascular network surrounding the conversion tanks is extremely dense. The coolant is circulated by a pump module which is located sternoventrally from the conversion tanks—separated by the filtration system which clears any obvious debris from the energy matrix fluid after conversion—and is powered by a separate, redundant battery array designed to maintain coolant flow in the event of major power loss. Circulatory fluid reservoirs flank the coolant pump module and are protected by internal armour shell plating.

Circulatory systems—both fuel and coolant—are regulated by the autonomic array of the central neuroprocessor (neurocable bus 8 and 9).

2ii. Approach to the Patient with Possible Circulovascular Malfunction

The first and most important aspect of circulovascular care is to verify that the circulation of fluids is unimpeded. Without proper circulation of coolant, vital systems will begin to overheat and shut down, and potential permanent damage may result. In some cases of circulatory failure, cooling is completely referred to the oxygen intakes; thus, the patient may present with oxygen intake distress as well as temperature spikes and localized or general system failure. It is important to determine whether oxygen intake distress is secondary to circulation failure or caused by a separate malfunction; all cases of oxygen intake distress should be checked for circulatory function and monitored to ensure that the circulatory systems remain patent. If the circulation is compromised due to physical damage or blockage of the conduits, the patient must be stabilized and cooling maintained by external means while repairs on the vessels are carried out. Most cases of circulovascular derangement are due to mechanical trauma and the consequent loss of circ fluid, but pathogenic involvement remains a possibility and must be investigated if symptoms and scan results warrant it.

Supportive therapy during the intense diagnostic phase consists of external auxiliary coolant and recirc connections, external power supply, and sedation via neurocircuitry block if shock—categorized by a sudden fall in vascular tension, fluctuation in central core temperature, and feedback loops in the autonomic control system—appears imminent.

  
2iii. Pump Function and Circulatory Control

As remarked above, the coolant is circulated via a shielded pump located in the main chest compartment ventral to the conversion tanks. This pump is run via neurocable bus 8, which traverses down the spinal column and is accessible via the cervical access panel before it splits into cable bunches to feed the systems of the upper torso. The connections with the local circuitry occur just below the split, and are difficult to access without cableties and retractors. The anatomy of the neurocable bundles should be familiar to the student of cybermedicine, but for reference a diagram is provided at the end of this chapter.

The pump itself is a simple and elegant piece of machinery which works on a two-chambered suction principle: returning coolant enters the first chamber as the second chamber is emptied, then the central valve closes as the second chamber fills; when it is full, the central valve opens to permit the coolant to flow into the second chamber under pressure, until the presseals are at their set limit, whereupon the interchamber valve shuts, the second chamber is emptied, and the circuit begins again. The pump is set at baseline to run at a certain rate, which may be overridden by increased cooling demands from the somatic systems due to exertion, temperature change, or pathogenic involvement. There are cascade failsafes guarding the operational circuitry for the pump, but in case of complete systemic failure it can be restarted by connecting a GS7 power coupling to the connector on the outside of the pump housing (anterior oblique connector 5). It is wise, in any case presenting with acute circ-pump failure, to check the circ fluid itself for the presence of foreign nanorobotic matter which may be causing malfunctions.

2iv. Hypertension

As noted above, the recirculating coolant fluid is contained within a vascular network, the tension of which is normally under autonomic control (neurocable bus 8). However, this control may be deranged due to energy overload (as in cases of electric shock) or stress. In rare cases, idiopathic vascular tension fluctuations have been noted; these are often ascribed to secondary circuit fluctuations consequent to minor system shock. Pathogens (q.v.) are capable of damaging the neurocircuitry which controls vascular tension; specifically, DHX-1 and CR-alpha have been recorded as producing tension fluctuations which cause secondary system malfunctions. Hemicrania (q.v.) also involves changes in cerebrovascular tension which are not fully understood, but which are believed to be associated with overstress in certain cerebral network bundles.

2v. Atherosclerosis-Thrombosis and Vascular Structure

The thrombotic subclassification of the CLA (q.v.) is limited in its actions, in normal functioning, to the repair of breached vessels. Local sensors in the vascular wall relay damage signals to the cerebral circuitry, which activates the thrombic CLA and directs them to the damaged area to repair the vascular wall. However, these signals may be spuriously activated by pathogenic or physical damage to the neural net. In certain degenerative neurocircuitry disorders, atherosclerosis of the vascular network may develop due to overactivation of the thrombic CLA despite the lack of vascular breach. Illegal substances such as "syk" also derange the normal functioning of neurocircuitry controlling vascular tension, and may cause permanent damage.

The vascular network itself is constructed of three layers of delicate myocircuitry. The inner and outer layers run transverse around the central layer, which runs longitudinally up the length of the vessel itself. Each of these layers is capable of contraction and expansion both locally and generally, under the control of the neurocable bunches for that particular sector. This flexibility allows for the preservation of the vascular integrity despite vessel breach in any given sector; the damaged area is contracted to shutdown by the local myocircuitry, while flow is resumed in subsidiary vessels to maintain cooling in the surrounding systems. All vascular breaches must be repaired as soon as possible to avoid the danger of localized overheating and circuitry damage subsequent to vessel damage.

Atherosclerosis may, as referenced above, be caused by damage to the autonomic immune system circuitry. The second major cause of atherosclerosis is inappropriate fuel additives; certain performance-enhancing additives contain large quantities of incontrovertible substances that are unfortunately able to pass through the filtration core between the conversion module and the circ-fluid reservoirs. These substances adhere to the vascular walls and integrate thrombic CLA bodies to form plaques of hard material which grow to sclerose the vascular lumen. Ultrasonic thrombotripsy may be useful in breaking up these plaques and releasing them for the detritophagic CLA to dispose of; otherwise, physical debridement of the vascular lumen is indicated, which may involve major surgery if the vessel involved is a deep one. At-risk patients must be counseled about the dangers of performance enhancers, both immediate and long-term.


	2. Circulating Leukocyte Analogues

3. Components of the Autonomic Immune System

In the Cybertronian model, the immune system is a collection of subroutines designed to protect the individual from damage caused by pathogens and foreign materials. In many ways it mirrors the humanoid immune system, particularly in the case of the _circulating leukocyte analogues_ (CLA), self-repairing nanobots found in the circ fluid which are segregated into three categories: _detritophagous_ (dCLA), _thrombic_ (tCLA), and _pathocidal_ (pCLA). The nomenclature here is flawed, as thrombic activity in organic systems is limited to platelets rather than leukocytes, but the circulating nanobots tasked with repairing vessel breaches are indicated as tCLA in order to minimize confusion.

3i. Detritophagous CLA

dCLA are the second most common of the circulating leukocyte analogues, and are responsible for two main functions: firstly, as the name implies, to consume and neutralize any foreign bodies or unnecessary fragments of thrombic material in the circ fluid; secondly, to produce more CLA as required by the immune system as a whole. Given the fact that the dCLA are constantly intaking material at the nanometric level, they are provided with a steady supply of raw material for the construction of new CLA. The entire CLA population is replaced roughly every three Galactic standard months.

Derangements in the dCLA, either structurally or in terms of numbers, can cause several troublesome conditions. If the subroutines that govern production of dCLA are damaged, overproliferation of dCLA (hyperdetritophagemia) can result: these superfluous dCLA then consume the other circulating bodies in the system and lower overall resistance to pathogenic intrusion. In addition, in extreme cases it has been verified that the dCLA begin to consume the actual vessel walls, which can lead to catastrophic structural failure and massive coolant loss. Symptoms of dCLA overproliferation may be slight to negligible until serious damage has been done; therefore, in any case in which dCLA overproliferation is suspected, it is vital to sample the circ fluid and run CLA counts as soon as possible. Waste products from the dCLA nanobotic construction process can also affect the coolant fluid's ability to transfer heat, and may cause the individual to present with a fluctuating overtemp that manifests on a twelve-hour cycle, as the dCLA levels in the circ fluid increase and decrease with the production of new dCLA. The importance of CLA counts in any overtemp condition cannot be overstressed, as this is often the first symptom of dangerous systemic derangement.

Certain conditions, such as contamination of the circ fluid or failure of the pathocidal CLA, can cause underproliferation of dCLA (hypodetritophagemia): this results in a buildup of detritus and chemical imbalances in the circ fluid, as well as an exponential drop in pCLA count, which places the individual at serious risk for pathogenic invasion. Buildup of detritus in the coolant lowers its heat-transfer coefficient and places a strain on secondary heat-transfer mechanisms; this often manifests as a temp control issue, with or without oxygen intake distress, which again should be addressed at once with circ fluid samples and CLA counts.

3ii. Thrombic CLA

The tCLA provide constant internal protection against vessel breach and damage. In the event of accidental or pathogenic vessel breach, the immune subroutines activate tCLA which bind to the edges of the breach and seal it while constructing new myocircuitry to restore the vessel to its original status. They are produced by the dCLA in response to chemical balances in the coolant fluid: a drop in the tCLA chemical signature activates dCLA subroutines to construct additional tCLA. Overproliferation of tCLA (hyperthrombicemia) can cause venous thrombosis and atherosclerosis, generally precipitated by pathogenic derangement of the dCLA which in normal functioning consume and neutralize any excess tCLA. As mentioned above, derangement of dCLA balances is likely to produce systemic power-cooling mismatch conditions manifesting in cyclic overtemp and heat-transfer stress; excess tCLA should be suspected in patients presenting with consistent hypertension and variable overtemp, and counts should be done on all potential hyper-tCLA conditions. Underproliferation of tCLA (hypothrombicemia) places the patient at risk for massive coolant loss with even slight vessel breaching, and any tendency to slow vessel repair and continual coolant loss should be followed up with CLA analysis and counts.

3iii. Pathocidal CLA

The pCLA are often considered the most important of the three subclassifications, as their role is to destroy any foreign or pathogenic intruders within the circ fluid. The immune system records the chemical and physical signature of any pathogen encountered by the pCLA for future reference, and if the pathogen is encountered a second time, the immune response produced by the pCLA will naturally be more rapid and comprehensive given its experience with the pathogenic profile. The science of cybernetic vaccinology is still in its infancy, but studies are underway to determine the viability of vaccines for such pathogens as DHX-1 and Alpha 7; if these studies provide positive results, the potential exists for full eradication of DHX-1 from the galaxy within the next ten years.

Overproliferation of pCLA can be prompted by massive pathogenic or foreign intrusion, as occurs in comprehensive physical damage and vessel breaching: in an otherwise functional individual, this is quickly brought under control as the dCLA engage in reuptake of unnecessary circulatory bodies, but in an immune-compromised individual can quickly spiral into a toxic condition known as hyperpathocidemia. The chemicals produced by the massive numbers of pCLA drastically lower the coolant's heat transfer coefficient, producing severe hyperthermia capable of causing malfunctions in cerebral circuitry: delirium, followed by coma as the cerebral functions trip offline, will occur, and if the hyperpathocidemia is not addressed may proceed further to permanent cerebral damage and deactivation. Hyperpathocidemia must be addressed quickly: emergency treatment consists of total support by external cooling and power lines, deactivation of the pathogen responsible for the initial response, and flushing of the entire coolant circuit to return the CLA balance and chemical composition to nominal. Once this has been accomplished, the immune deficiency or hyperreaction which precipitated the episode of hyperpathocidemia may be addressed. The most important aspect of treating this condition is to maintain cooling to the cerebral circuitry, as heat damage here may not be survivable.

Underproliferation of pCLA (hypopathocidemia) is generally caused by malfunctioning dCLA, and places the individual at risk for massive pathogenic invasion and systemic toxic shock. As the pCLA levels in the circ fluid are not sufficient to mount an appropriate response to the invading pathogen, there is no rapid progression of hyperthermia as in hyperpathocidemia: instead, the effects of the pathogen itself will decrease the efficiency of the coolant fluid and cause a slow but steady rise in temperature and systemic distress. Chemical and thermal imbalances caused by this pathogenic load will manifest themselves in many different subsystems, including the automatic toxin protection system (offloading of fuel from conversion and holding tanks), the gyrostability system (vertigo, disorientation), the oxygen subsidiary cooling circuits (oxygen intake distress), and the neurosensory damage notification system (algesia). As the patient may not be aware of his or her hypopathocidemic condition, these symptoms may come on suddenly, and result in a presentation of multiple systemic failure which can often cause serious psychological distress; for this reason it is important to reassure the patient and attempt to reduce psychological involvement, as this in itself can increase stress-related systemic derangement. Immediate response to the hypopathocidemic patient with a fulminant infection requires total systemic support: sedation via neurocircuitry block may be necessary if the algesia and fuel offloading subroutines go into seizure loops. Matching pCLA should be administered while monitoring vital functions, and a full coolant circuit flush may be necessary to remove the infection completely in cases of very low pCLA production.

Individuals with CLA imbalance should undergo neurocircuitry examination to determine the faulty subroutine in the immune programming which is causing the imbalance, and if necessary undergo total immune reprogramming; this is not desirable, as it places the patient at risk during reprogramming, and constant supportive monitoring must be provided until reprogramming is complete.


End file.
